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Integrins mediate mechanical compression-induced endothelium-dependent vasodilation through endothelial nitric oxide pathway.

Lu X, Kassab GS - J. Gen. Physiol. (2015)

Bottom Line: We cannulated isolated swine (n = 39) myocardial (n = 69) and skeletal muscle (n = 60) arteriole segments and exposed them to cyclic transmural pressure generated by either intraluminal or extraluminal pressure pulses to simulate compression in contracting muscle.It was attenuated by inhibition of NO synthase and by mechanical removal of the endothelium.We therefore conclude that integrin plays a role in cyclic compression-induced endothelial NO production and thereby in the vasodilation of small arteries during cyclic transmural pressure loading.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Biomedical Engineering, Department of Cellular and Integrative Physiology, Department of Surgery, and Indiana Center for Vascular Biology and Medicine, Indiana University-Purdue University Indianapolis, Indianapolis, IN 46202.

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Role of integrins in the cyclic transmural pressure–induced vasodilation. (A) RGD peptide (GRGDSP) incubated with the vessel segments for 60 min prevented the vasodilation induced by the cyclic transmural pressure. (B) Control RGE peptide (GRGESP) did not affect the cyclic transmural pressure–induced vasodilation. (C) Function-blocking integrin α5β1 or αvβ3 antibodies compromised the cyclic transmural pressure–induced vasodilation. The top two panels represent the coronary arteries, and bottom two panels represent the skeletal muscle arteries. The vessel segments were incubated with function-blocking integrin α5β1 and αvβ3 antibodies, which were continuously administrated into lumen with a microsyringe pump.
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fig4: Role of integrins in the cyclic transmural pressure–induced vasodilation. (A) RGD peptide (GRGDSP) incubated with the vessel segments for 60 min prevented the vasodilation induced by the cyclic transmural pressure. (B) Control RGE peptide (GRGESP) did not affect the cyclic transmural pressure–induced vasodilation. (C) Function-blocking integrin α5β1 or αvβ3 antibodies compromised the cyclic transmural pressure–induced vasodilation. The top two panels represent the coronary arteries, and bottom two panels represent the skeletal muscle arteries. The vessel segments were incubated with function-blocking integrin α5β1 and αvβ3 antibodies, which were continuously administrated into lumen with a microsyringe pump.

Mentions: To assess the role of integrins, we investigated the effect of RGD peptide and the function-blocking integrin α5β1 and αvβ3 antibodies on the cyclic transmural pressure–induced vasodilation. RGD peptides competitively combine with integrin to attenuate mechanical stimuli–induced integrin activation (Mogford et al., 1997; Schlaepfer and Hunter, 1997; Yip and Marsh, 1997; Platts et al., 1998). In Fig. 4 A, using a typical sample of diameter tracings, we show that the preincubation of the vessel segments with RGD peptide inhibited the cyclic transmural pressure–induced vasodilation. GRGESP (a control RGE peptide) did not attenuate the cyclic transmural pressure-induced vasodilation (Fig. 4 B). The diameter tracings of the vessel segments preincubated with the function-blocking integrin α5β1 or αvβ3 antibodies also show that the antibodies attenuated the cyclic transmural pressure–induced vasodilation (Fig. 4 C).


Integrins mediate mechanical compression-induced endothelium-dependent vasodilation through endothelial nitric oxide pathway.

Lu X, Kassab GS - J. Gen. Physiol. (2015)

Role of integrins in the cyclic transmural pressure–induced vasodilation. (A) RGD peptide (GRGDSP) incubated with the vessel segments for 60 min prevented the vasodilation induced by the cyclic transmural pressure. (B) Control RGE peptide (GRGESP) did not affect the cyclic transmural pressure–induced vasodilation. (C) Function-blocking integrin α5β1 or αvβ3 antibodies compromised the cyclic transmural pressure–induced vasodilation. The top two panels represent the coronary arteries, and bottom two panels represent the skeletal muscle arteries. The vessel segments were incubated with function-blocking integrin α5β1 and αvβ3 antibodies, which were continuously administrated into lumen with a microsyringe pump.
© Copyright Policy - openaccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4555471&req=5

fig4: Role of integrins in the cyclic transmural pressure–induced vasodilation. (A) RGD peptide (GRGDSP) incubated with the vessel segments for 60 min prevented the vasodilation induced by the cyclic transmural pressure. (B) Control RGE peptide (GRGESP) did not affect the cyclic transmural pressure–induced vasodilation. (C) Function-blocking integrin α5β1 or αvβ3 antibodies compromised the cyclic transmural pressure–induced vasodilation. The top two panels represent the coronary arteries, and bottom two panels represent the skeletal muscle arteries. The vessel segments were incubated with function-blocking integrin α5β1 and αvβ3 antibodies, which were continuously administrated into lumen with a microsyringe pump.
Mentions: To assess the role of integrins, we investigated the effect of RGD peptide and the function-blocking integrin α5β1 and αvβ3 antibodies on the cyclic transmural pressure–induced vasodilation. RGD peptides competitively combine with integrin to attenuate mechanical stimuli–induced integrin activation (Mogford et al., 1997; Schlaepfer and Hunter, 1997; Yip and Marsh, 1997; Platts et al., 1998). In Fig. 4 A, using a typical sample of diameter tracings, we show that the preincubation of the vessel segments with RGD peptide inhibited the cyclic transmural pressure–induced vasodilation. GRGESP (a control RGE peptide) did not attenuate the cyclic transmural pressure-induced vasodilation (Fig. 4 B). The diameter tracings of the vessel segments preincubated with the function-blocking integrin α5β1 or αvβ3 antibodies also show that the antibodies attenuated the cyclic transmural pressure–induced vasodilation (Fig. 4 C).

Bottom Line: We cannulated isolated swine (n = 39) myocardial (n = 69) and skeletal muscle (n = 60) arteriole segments and exposed them to cyclic transmural pressure generated by either intraluminal or extraluminal pressure pulses to simulate compression in contracting muscle.It was attenuated by inhibition of NO synthase and by mechanical removal of the endothelium.We therefore conclude that integrin plays a role in cyclic compression-induced endothelial NO production and thereby in the vasodilation of small arteries during cyclic transmural pressure loading.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Biomedical Engineering, Department of Cellular and Integrative Physiology, Department of Surgery, and Indiana Center for Vascular Biology and Medicine, Indiana University-Purdue University Indianapolis, Indianapolis, IN 46202.

Show MeSH
Related in: MedlinePlus